Genetics target site insensitivity

The existence of multiple AChE isoenzymes has several consequences. First, it increases the chances of an insect having one that is, or by a minor genetic change can be rendered, insensitive. The molecular redundancy combined with a selection pressure in the form of persistent insecticide applications would facilitate target site resistance development. Second, it could be a factor in the frequent lack of target site cross resistance between OPs and carbamates, and even between different OPs. Third, it would facilitate the disappearance of the insensitive form(s) in the absence of a selection pressure. This would especially easily explain observed instability of resistance if the form(s) with decreased affinity for the inhibitors also have decreased affinity for the neurotransmitter. Insensitivity to the inhibitor may be accompanied by a reduced rate of neurotransmitter hydrolysis (56. 28), but this is not always the case. It seems that the reduced rate of neurotransmitter hydrolysis does not impair survival, at least in laboratory cultures of insects. It is unclear what impact such reduced rates have in field populations. 

During resistance studies with Alopecurus myosuroides populations from the UK two biotypes, Oxford A1 and Notts. Al, were identified, which were highly resistant to fenoxaprop, didofop, fluazifop and sethoxydim due to an insensitive ACCase. Genetic studies revealed that the target-site resistance in the two A. myosuroides biotypes was monogenic and nuclear inherited, with the resistant allele showing complete dominance [38]. 

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